About Me

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Since the discovery of prion diseases, the concept has emerged that a
protein could be a transmissible pathogen. As such, this transmissible pathogen
agent can transfer its pathological mis-folded shape to the same but normally
folded protein thus leading to the propagation of a disease. This idea is now
extrapolated to several neurological diseases associated with protein
mis-folding and aggregation, such as Alzheimer’s disease (AD). AD is a slowly
developing dementing disease characterized by the coexistence of two types of
lesions: the parenchymal amyloid deposits and the intraneuronal neurofibrillary
tangles (NFT). Amyloid deposits are composed of amyloid-beta peptides that
derive from sequential cleavages of its precursor named amyloid protein
precursor. NFT are characterized by intraneuronal aggregation of abnormally
modified microtubule-associated Tau proteins. A synergistic relationship between
the two lesions may trigger the progression of the disease. Thus, starting in
the medial temporal lobe and slowly progressing through temporal, frontal,
parietal, and occipital cortex, the spreading of NFT is well correlated with
clinical expression of the disease and likely follows cortico-cortical neuronal
circuitry. However, little is known about the mechanism driving the
spatiotemporal propagation of these lesions ultimately leading to the disease. A
growing number of studies suggest that amyloid deposits and NFT are resulting
from a prion-like spreading. In the present chapter, we will develop the current
hypotheses regarding the molecular and cellular mechanisms driving the
development and spreading of AD lesions from the window of multivesicular
endosomes/bodies and exosomes.

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both disease, and it’s variants, in many cases are merely
names of the people that first discovered them. Both diseases are incurable and
debilitating brain disease, that are in the end, 100% fatal, with the
incubation/clinical period of the Alzheimer’s disease being longer than the TSE
prion disease. Symptoms are very similar, and pathology is very similar. I
propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation
disease, and that Alzheimer’s is Transmissible, and is a threat to the public
via the many Iatrogenic routes and sources. It was said long ago that the only
thing that disputes this, is Alzheimer’s disease transmissibility, or the lack
of. today, there is enough documented science (some confidential), that shows
that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and
or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and
one that needs to be addressed immediately.

Methods

Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.

Results

The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you
can take the ash and mix it with saline and inject that ash into a mouse, and
the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still
Infectious after Biodiesel Production as well. the TSE prion agent also survives
Simulated Wastewater Treatment Processes. IN fact, you should also know that the
TSE Prion agent will survive in the environment for years, if not decades. you
can bury it and it will not go away. TSE prion agent is capable of infected your
water table i.e. Detection of protease-resistant cervid prion protein in water
from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it
out and be done with. that’s what’s so worrisome about Iatrogenic mode of
transmission, a simple autoclave will not kill this TSE prion agent.

Conclusions

There should be a Global Congressional Science round table event (one of
scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics let science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already. what’s the use of science progressing human life to
the century mark, if your brain does not work?

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both diseases are incurable and debilitating brain disease,
that are in the end, 100% fatal, with the incubation/clinical period of the
Alzheimer’s disease being longer (most of the time) than the TSE prion disease.
Symptoms are very similar, and pathology is very similar.

Methods

Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.

Results

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long
incubation disease, and that Alzheimer’s is Transmissible, and is a threat to
the public via the many Iatrogenic routes and sources. It was said long ago that
the only thing that disputes this, is Alzheimer’s disease transmissibility, or
the lack of. The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease.

Conclusions

There should be a Global Congressional Science round table event set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics lets science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already.

Ample justification exists on clinical, pathologic, and biologic grounds
for considering a similar pathogenesis for AD and the spongiform virus
encephalopathies. However, the crux of the comparison rests squarely on results
of attempts to transmit AD to experimental animals, and these results have not
as yet validated a common etiology. Investigations of the biologic similarities
between AD and the spongiform virus encephalopathies proceed in several
laboratories, and our own observation of inoculated animals will be continued in
the hope that incubation periods for AD may be even longer than those of CJD.

Our results suggest that some of the typical brain abnormalities associated
with AD can be induced by a prion-like mechanism of disease transmission through
propagation of protein misfolding. These findings may have broad implications
for understanding the molecular mechanisms responsible for the initiation of AD,
and may contribute to the development of new strategies for disease prevention
and intervention. Keywords: amyloid; prion; protein misfolding; disease
transmission

# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy
prion disease, Iatrogenic, what if ? and the opportunity to present it, at the
Alzheimer’s Association International Conference 2012 (AAIC), as a poster
presentation. However, with great sadness, I must regretfully decline the
invitation due to a medical reasons, and traveling to Canada, of which is not
possible. ...

Thank You,

With Kindest Regards,

I am sincerely,

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

flounder9@verizon.net

From:

Sent: Saturday, April 07, 2012 8:20 PM

To: Terry S. Singeltary Sr.

Subject: RE: re-submission

Dear Terry,

Yes, your proposal was accepted as a poster presentation. Please decline
the invitation if appropriate.